Skip to main content
padlock icon - secure page this page is secure

Macrophage‐Related Demyelination In Peripheral Nerves Of Mice Deficient In The Gap Junction Protein Connexin 32

Buy Article:

$52.00 + tax (Refund Policy)

Mice deficient in the gap junction protein connexin 32 (Cx32) develop a slowly progressing demyelinating neuropathy, with enlarged periaxonal collars, abnormal non‐compacted myelin domains and axonal sprouts. These mice serve as a model for the X‐linked form of inherited demyelin‐ ating neuropathies in humans. Based on our previous findings that macrophages are involved in demyelination in other myelin mutants (i.e. mice heterozygously deficient in P0), we considered the possibility that macrophages might be also mediators of demyelination in Cx32‐deficient mice. Indeed, we detected an age‐related increase in the number of macrophages in demyelinating nerves of Cx32‐deficient mice. In addition, immunoelectron microscopy revealed macrophages in an apposition to degenerating myelin reminiscent of a macrophage‐mediated demyelinating neuropathy. We conclude that involvement of macrophages might be a widespread phenomenon in genetically‐determined demyelination.
No References
No Citations
No Supplementary Data
No Article Media
No Metrics

Document Type: Research Article

Affiliations: .

Publication date: September 1, 2002

  • Access Key
  • Free content
  • Partial Free content
  • New content
  • Open access content
  • Partial Open access content
  • Subscribed content
  • Partial Subscribed content
  • Free trial content
Cookie Policy
Cookie Policy
Ingenta Connect website makes use of cookies so as to keep track of data that you have filled in. I am Happy with this Find out more